Three separate hypotheses are presented for a molecular description of the events which occur to produce a shouldered radiation survival curve. (1) The lethal event is a double strand break, the yield of which increases with post-irradiation time due to hydrolysis of labile bonds. With increasing dose, the repair system becomes saturated and more potential breaks become actual breaks, hence the shoulder. In this case, Elkind-Sutton repair is the complete expression of the potential damage. (2) Sulfhydryl compounds, active in chemical repair, are depleted by increasing radiation doses and cells become more sensitive. Non-protein sulfhydryls and/or protein bound sulfhydryls could be involved. Here Elkind-Sutton repair is the re-establishment of pre-irradiation SH levels. (3) A significant repair enzyme, DNA polymerase, is consumed by binding irreversibly to radiation damaged sites on DNA. With increasing dose, less repair is possible so cells become more sensitive. Again, Elkind-Sutton repair is re-establishment of pre-irradiation polymerase levels. Experiments are proposed to test these hypotheses both in vitro - aqueous solution radiation chemistry and in vivo - using cells which have characteristic shouldered response HeLa and CHO.